Lung surfactant production in the developing fetus is being studied by assessment of its principal phospholipid component, phosphatidylcholine (PC). The primary mechanism for lung PC synthesis has been identified as the choline pathway. The first enzyme of this pathway, choline kinase, has been shown to be substrate activated. The choline concentrations in the fetal lung have therefore been determined at various gestational ages. The enzyme was also demonstrated to be activated by polyamines. Lung PC concentration and choline pathway rates have been shown to increase during the latter 10-20% of gestation in many fetal species. These changes may be induced by administration of corticosteroids. As the polyamines have been demonstrated to be mediators of hormone action in other developing tissues, a similar mechanism may exist in lung. Thus, corticosteroids, mediated by polyamines, may provide the stimulus for PC biosynthesis. Promising data from clinical trials elsewhere suggest that corticosteroids may be useful in the prevention of the respiratory distress syndrome of human neonates.